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PMID: 19785921 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Review

Bidirectional signaling of ErbB and Eph receptors at synapses.

Neuron glia biology ·Vol. 4 ·No. 3 ·2008-08-00 ·Pages 211-21

Chen Y, Fu AK, Ip NY

Abstract

Synapse development and remodeling are regulated by a plethora of molecules such as receptor tyrosine kinases (RTKs), a family of cell surface receptors that play critical roles in neural development. Two families of RTKs implicated in synaptic functions, ErbBs and Ephs, share similar characteristics in terms of exhibiting forward and reverse signaling. In this review, we will discuss the latest advances in the functions of ErbBs and Ephs at the synapse, including dendritic spine morphogenesis, synapse formation and maturation, and synaptic transmission and plasticity. In addition to signaling at interneuronal synapses, communication between neuron and glia is increasingly implicated in the control of synaptic functions. Studies on RTKs and their cognate ligands in glial cells enhance our understanding on the nature of 'tripartite synapse'. Implications of these signaling events in human diseases will be discussed.

MeSH Terms
Animals Ephrins/metabolism Humans Mental Disorders/metabolism Models, Biological Neuroglia/physiology Neuronal Plasticity/physiology Receptor, EphA1/physiology Receptor, ErbB-2/physiology Signal Transduction/physiology Synapses/physiology Synaptic Transmission/physiology gamma-Aminobutyric Acid/metabolism
Chemicals
Ephrins gamma-Aminobutyric Acid Receptor, EphA1 Receptor, ErbB-2
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Chen Yu
Department of Biochemistry, Molecular Neuroscience Center and Biotechnology Research Institute, Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong, China.
Fu Amy K Y
Ip Nancy Y
Article Info
Journal
Neuron glia biology
Abbr.
Neuron Glia Biol
ISSN
1741-0533
Published
2008-08-00
Epub
2009-00-29
Pages
211-21
Language
English
Region
England
NLM ID
101217278
Subset
IM
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